Of further note is the occurrence of genetic polymorphism in the SOCS-1 gene where a particularly significant association has been found between asthma susceptibility and a promotor polymorphism which was shown to cause increased transcription of SOCS-1. Thus, there is a potential for gene-gene interactions involving polymorphisms in the TGFB2 and SOCS1 genes linked to virus-induced asthma exacerbations. In conclusion, our data suggest that higher levels of endogenous TGF-b expression contribute to the decreased innate immune Paclitaxel side effects response to virus infection in asthmatic epithelial cells. This involved reduction of both IFN-b and IFNl1/IL-29 mRNA and protein expression in response to RV infection and was mirrored by similar responses when the cells were exposed to the TLR3 agonist, poly IC. This response was associated with higher endogenous levels of TGF-b2 protein and elevated SOCS1 and SOCS3 expression that could be down-regulated. Although not investigated directly, our data suggest that genetic polymorphisms in either the TGFB2 or SOCS-1 gene may dictate varying degrees of susceptibility to virus infection in asthma. There is also the possibility that production of other isoforms of TGF-b by cell types such as eosinophils, whose numbers are increased in asthmatic bronchial epithelium during rhinovirus colds and persist during convalescence, may also directly contribute to virus-induced exacerbations by affecting the ability of epithelial cells to mount an adequate innate anti-viral immune response. The aim of this therapy is, amongst others, to shrink the tumour before surgery to increase the probability of complete resection and to thus improve patient survival. However, response rates are low, and complete or subtotal tumour regression is observed in only 20–40% of the patients. Thus, chemotherapy resistance is a major obstacle for successful treatment. According to the cancer stem cell hypothesis, tumour cells are heterogeneous, and an increased drug resistance is a particular phenotype of a minority of tumour cells – the so-called cancerinitiating cells or cancer stem cells. An increase in the CSC population after chemotherapy has been demonstrated, and stem cell based gene expression signatures were associated with poor prognosis in various tumours including gastric carcinomas. The CSC hypothesis is still controversially discussed, but there is evidence for the existence of CSCs in several tumour types and molecular markers have been identified which are preferentially found on these cells. The activation of embryonic signalling pathways, such as the Wnt, Notch and Hedgehog pathways, has been suggested as a driving force for the formation of CSCs. Data regarding the source and existence of gastric CSCs remain inconclusive. In mice, bone-marrow derived cells or a specific cell population in the antrum expressing the Wnt target molecule LGR5, have been associated with CSCs in the stomach. In addition, CD44 and CD24 have been suggested as specific cell surface markers, but the data are inconsistent. The neoadjuvant treatment protocol for GC provides an excellent opportunity to investigate tumour cells before and after chemotherapy in patients. In this study, we aimed to elucidate first, whether the expression of putative CSC-related genes in the posttherapeutic residual tumour predicts patient survival and second, whether particular genes are differentially expressed between pretherapeutic biopsies and the post-therapeutic tumour specimens, consistent with an enrichment of chemotherapy-resistant tumour cells as predicted by the CSC concept.